In GERD, FUT4-mediated fucosylation critically regulates the function of adhesion molecules, such as CD44, by modifying their glycostructures, which can alter cell–cell and cell–matrix interactions.[44] The observed upregulation of FUT4 may lead to aberrant fucosylation of membrane proteins on esophageal epithelial cells, potentially disrupting the assembly and function of tight junctions, thereby impairing mucosal cohesion and repair, and rendering the epithelium more vulnerable to acid and pepsin injury. The gene discussed is FUT4; the disease is gastroesophageal reflux disease.